Abstract

Background: The ability to scavenge reactive oxygen species (ROS) is crucial for cornea epithelial cells to resist oxidative damage. The authors previously demonstrated that exogenous thymosin beta-4 (Tβ₄) was able to protect human cornea epithelial (HCE-T) cells against H₂O₂-induced oxidative damage, and its cellular internalisation was essential. The aim of this study is to further elucidate its protective mechanism.

Methods: HCE-T cells with or without Tβ₄ pretreatment were exposed to H₂O₂, and the differences in caspase activity, intracellular ROS levels, cell viability, and the expression of anti-oxidative enzymes, were measured and compared.

Results: Besides reducing caspase-9 activation and intracellular ROS levels induced by H₂O₂, treatment of Tβ₄ could also increase cell viability and stimulate the expression of manganese superoxide dismutase (SOD) and copper/zinc SOD. Moreover, both transcription and translation levels of catalase were also upregulated by Tβ₄ in the presence of exogenous H₂O₂. Furthermore, it was demonstrated that the addition of catalase inhibitor abrogated the protective effect of Tβ₄ against H₂O₂-induced oxidative damage.

Conclusion: To the best of the authors' knowledge, this is the first report to show that Tβ₄ was capable of upregulating anti-oxidative enzymes in human corneal epithelial cells, and these findings further support its role in cornea protection.